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Featured researches published by S. Wagner.


Digestive Diseases and Sciences | 2000

Helicobacter pylori Reduces Intracellular Glutathione in Gastric Epithelial Cells

Winfried Beil; Barbara Obst; Karl-Friedrich Sewing; S. Wagner

Helicobacter pylori infection has been associated with stimulation of gastric mucosal reactive oxygen species (ROS) production, and it was postulated that ROS production is due to neutrophil infiltration and activation. The aim of this study was to investigate the direct effect of H. pylori on ROS formation in gastric epithelial cells in vitro. The human gastric cancer cell line HM02 was incubated with H. pylori for 24 hr, and the effects on cell number and the intracellular radical scavenger reduced glutathione (GSH) were assessed. H. pylori caused a concentration-dependent reduction of cellular GSH concentrations over a broad bacteria-to-cell ratio (1.4–42) in the absence of cell necrosis. The radical scavengers MnTBAP (a cell permeable superoxide dismutase) and ebselen provided protection against H. pylori-induced decrease in cellular GSH concentrations. We conclude that H. pylori directly decreases cellular GSH concentrations in gastric epithelial cells. We suggest that this effect is caused by the release of ROS by H. pylori.


European Radiology | 2000

Role of the intra-arterial calcium stimulation test in the preoperative localization of insulinomas.

Ajay Chavan; Timm Kirchhoff; Georg Brabant; G. F. W. Scheumann; S. Wagner; Michael Galanski

Abstract. The aim of this study was determination of the significance of the arterial stimulation test with venous sampling (ASVS) in the preoperative localization of insulinoma. Eleven patients with endogenous hyperinsulinism underwent preoperative transabdominal US, spiral computer tomography (spiral CT), MRI, endoscopic ultrasound (EUS) as well as angiography (DSA) combined with ASVS. The results were compared with intraoperative findings, intraoperative ultrasound (IOUS) and histopathology. There were no complications related to the ASVS test. In 11 patients the tumor could be localized with the various modalities as follows: US 1 of 11 (9 %), MRI 3 of 10 (30 %), spiral CT 4 of 11 (36 %), EUS 5 of 10 (50 %), DSA 8 of 11 (73 %), and ASVS 10 of 11 (91 %). In 2 patients the tumors were intraoperatively neither palpable nor detectable by IOUS, and consequently the intraoperative management was governed by information provided by DSA combined with the ASVS test. Ten patients had solitary benign insulinomas and 1 patient with multiple endocrine neoplasia I had two tumors adjacent to each other in the pancreatic tail. Arterial stimulation test with venous sampling was the most sensitive preoperative test for regionalizing the insulinoma in our set of patients. It can be performed safely in the course of a regular DSA examination and may affect intra-operative management in patients in whom the tumors are not detectable by palpation or IOUS.


Prostaglandins Leukotrienes and Essential Fatty Acids | 1998

Helicobacter pylori fatty acid cis 9,10-methyleneoctadecanoic acid increases [Ca2+]i, activates protein kinase C and stimulates acid secretion in parietal cells

Winfried Beil; C. Birkholz; S. Wagner; K.-Fr. Sewing

The effect of the Helicobacter pylori (H. pylori) fatty acid cis 9,10-methyleneoctadecanoic acid (MOA) on gastric acid secretion was studied in isolated guinea-pig parietal cells. MOA (1 and 3 micromol/l) stimulated basal and enhanced histamine- and dibutyryl cyclic AMP-stimulated acid secretion in parietal cells. MOA increased intracellular free [Ca2+]i concentration in a concentration-dependent manner. The source of [Ca2+]i was extracellular as demonstrated by depletion of [Ca2+]i with EGTA. Furthermore, MOA caused activation of parietal cell protein kinase C (PKC). The effect of MOA upon PKC activation was [Ca2+]i-dependent but did not require phosphatidylserine as phospholipid co-factor. Similarly to the effect of diolein, MOA increased the stimulatory effect of phosphatidylserine at low [Ca2+]i concentrations. Treatment of parietal cells with MOA caused translocation of PKC from the cytosol to the membrane-associated cell fraction. We propose that MOA stimulates parietal cell acid secretion presumably by an increase of cytosolic free [Ca2+]i concentrations and PKC activation.


Carcinogenesis | 2000

Helicobacter pylori causes DNA damage in gastric epithelial cells

B. Obst; S. Wagner; K.F. Sewing; W. Beil


European Radiology | 2004

Hepatic artery embolization for treatment of patients with hereditary hemorrhagic telangiectasia and symptomatic hepatic vascular malformations

Ajay Chavan; Martin Caselitz; Karl-Friedrich Gratz; Joachim Lotz; Timm Kirchhoff; Plinio Piso; S. Wagner; Michael P. Manns; Michael Galanski


Gastroenterology | 1999

Octreotide for therapy of chylous ascites in yellow nail syndrome

Adji Widjaja; K.F. Gratz; Johann Ockenga; S. Wagner; Michael P. Manns


Microbial Pathogenesis | 2002

Helicobacter pylori -induced apoptosis in gastric epithelial cells is blocked by protein kinase C activation.

Barbara Obst; Silke Schütz; Susanne Ledig; S. Wagner; Winfried Beil


Archive | 2001

Helicobacter pylori augments the acid inhibitory eVect of omeprazole on parietal cells and gastric

Winfried Beil; K-F Sewing; R Busche; S. Wagner


Gastroenterology | 1998

Helicobacter pylori and its fatty acids differentially increase intracellular Ca2+ in gastric epithelial cells

S. Wagner; T. Feske; Winfried Beil; Michael P. Manns; C. Schöfl


Gastroenterology | 1998

Helicobacter pylori attenua tes sulfhydryl levels in the gastric cell line HM02

Winfried Beil; S. Wagner; Barbara Obst; Gabriele I. Kirchner; K.-Fr. Sewing

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Barbara Obst

Hannover Medical School

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Ajay Chavan

Hannover Medical School

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Adji Widjaja

Hannover Medical School

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C. Birkholz

Hannover Medical School

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